IgA nephropathy (IgAN) is the most common form of glomerulonephritis worldwide. IgAN progresses to end-stage kidney disease in 20-40% of patients within 20 years of diagnosis. Kidney transplantation is the most effective option for patients with end-stage kidney disease caused by IgAN, but recurrence can occur in the transplanted kidney. The IgAN recurrence rate varies from 1% to 10% per year, and varies according to the follow-up period, diagnostic modality, and biopsy criteria. Of note, studies based on protocol biopsies have reported a higher incidence of recurrence, which also occurred earlier after transplantation. In addition, recent data show that recurrence of IgAN is a more significant cause of allograft failure than previously believed. Little is known about the pathophysiology of IgAN recurrence, but several potential biomarkers have been investigated. Among them, galactose-deficient IgA1 (Gd-IgA1), IgG anti-Gd-IgA1 antibodies, and soluble CD89 could play a pivotal role in disease activity. This review aims to describe the current status of recurrent IgAN, including the incidence, clinical characteristics, risk factors, and future perspectives, with a focus on the available therapeutic approaches.

The three primary sites of acute T-cell mediated rejection (TCMR) in transplanted kidneys are the tubular epithelial cells, interstitum, and the vascular endothelial cells. The pathology of acute lesions is characterized by inflammatory cell infiltration; the final diagnosis suggested by the Banff 2019 classification is guided by grading of tubulitis (the t-score), interstitial inflammation (the i score), and endarteritis (the v score). Consistent major issues when using the Banff classification are the etiological classifications of interstitial fibrosis and tubular atrophy (IFTA). From 2015 to 2019, technological advances (i.e., genetic analysis in paraffin sections), increased our understanding of IFTA status in patients with smoldering acute TCMR and the roles played by inflammatory cell infiltration (the i-IFTA score) and tubulitis (the t-IFTA score) in IFTA. These two scores were introduced when establishing the diagnostic criteria for chronic active TCMR. Despite the increase in complexity and the lack of a consensus treatment for chronic active TCMR, the Banff classification may evolve as new techniques (i.e., genetic analysis in paraffin sections and deep learning of renal pathology), are introduced. The Banff conference proceeded as follows. First, lesions were defined. Next, working groups were established to better understand the lesions and to derive better classification methods. Finally, the new Banff classification was developed. This approach will continue to evolve; the Banff classification will become a very useful diagnostic standard. This paper overviews the history of TCMR diagnosis using the Banff classification, and the clinical importance, treatment, and prospects for acute and chronic active TCMR.

A 39-year-old woman with end-stage renal failure of unknown origin was on peritoneal dialysis for 10 years. One year ago, she underwent ABO-incompatible living-donor kidney transplantation from her husband. After the kidney transplantation, her serum creatinine level remained around 0.7 mg/dL, but her serum potassium level remained low at around 3.5 mEq/L despite potassium supplementation and spironolactone. The patient’s plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were markedly elevated (20 ng/mL/h and 868 pg/mL, respectively). A CT angiogram of the abdomen performed one year previously suggested stenosis of the left native renal artery, which was considered responsible for the hypokalemia. Renal venous sampling was done on both native kidneys and the transplanted kidney. Since renin secretion from the left native kidney was significantly elevated, a laparoscopic left nephrectomy was performed. Postoperatively, the renin-angiotensin-aldosterone system was markedly improved (PRA: 6.4 ng/mL/h, PAC: 147.3 pg/mL), and the serum potassium levels also improved. Pathological examination of the removed kidney showed many atubular glomeruli and hyperplasia of the juxtaglomerular apparatus (JGA) in residual glomeruli. In addition, renin staining showed strong positivity in the JGA of these glomeruli. Here, we report a case of hypokalemia caused by left native renal artery stenosis in a kidney transplant recipient. This valuable case study provides histological confirmation of maintained renin secretion in an abandoned native kidney after kidney transplantation.